Abstracts for the 60Th Annual Meeting of the Society for Investigative Dermatology Sheraton Chicago Hotel, Chicago, Illinois May 5–9, 1999
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View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector ABSTRACTS Abstracts for the 60th Annual Meeting of the Society for Investigative Dermatology Sheraton Chicago Hotel, Chicago, Illinois May 5–9, 1999 Plenary and Concurrent Sessions Abstract Numbers Plenary and Concurrent Sessions Abstract Numbers Plenary Session I 0001–0016 Posters Concurrent Minisymposia Aging 256–262, 542–548 Use of Dendritic Cells as Immunotherapeutic Agents 001–008 Bullous Disease 263–277, 549–563 Hair Follicle Morphogenesis/Carcinogenesis 009–016 Carcinogenesis 278–288, 564–574 Apoptosis 017–024 Cell Biology/Biochemistry 289–300, 575–585 Adhesion: Components and Mechanisms 025–032 (General) General Plenary Session 1 033–049 Cell Biology/Biochemistry 301–336, 586–621 Concurrent Oral Sessions (Keratinocyte) Bullous Disease 050–062 Cell Biology/Biochemistry 337–348, 622–632 Immunology/Inflammation–Cytokines,SolubleFactors 063–074 (Langerhans Cell/Lymphocyte) Extracellular Matrix/Connective Tissue 075–087 Cell Biology/Biochemistry 349–359, 633–642 Epidemiology/Health Services Research 088–100 (Melanocyte) Cell Biology/Biochemistry–Melanocytes 101–113 Dermatopathology/Morphology 360–371, 643–654 Lipids/Barrier Function 114–126 Extracellular Matrix/Connective 372–388, 655–672 Cell Biology/Biochemistry 127–139 Tissue Gene Expression 389–406, 673–689 General Plenary Session 2 140–154 Genetic Disease/Gene Therapy 407–424, 690–708 Concurrent Oral Sessions Growth Factors/Signal 425–438, 709–722 Gene Expression 155–166 Transduction Genetic Disease/Gene Therapy 167–178 Immunology/Inflammation 439–459, 723–743 Growth Factors/Signal Transduction 179–190 (Cellular) Immunology/Inflammation–Cellular 191–202 Immunology/Inflammation 460–481, 744–766 Carcinogenesis 203–215 (Cytokines, Soluble Factors) Cell Biology/Biochemistry 2 216–227 Photobiology 228–239 Infectious Disease/Virology 482–490, 767–774 Concurrent Minisymposia Lipids/Barrier/Percutaneous 491–467, 775–780 Growth Factors/Signal Transduction 240–247 Absorption Novel Therapeutic Strategies/Clinical Trials 248–255 Pharmacology/Clinical Trials 498–518, 781–800 Photobiology 519–541, 801–823 Epidemiology/Health Services Research 824–839 Committee on Scientific Programs, 1998–1999 Jack B. Longley, Thomas A. Luger, Kathi C. Madison, Estela E. Medrano, John C. Ansel, Leonard M. Milstone, Alice P. Pentland, Dennis R. Roop, Robert L. Modlin, Pauline M. Schwartz, Glynis Scott, Georg Stingl, Raija Chairman, Tung-Tien Sun, David R. Bickers (ex officio), David A. Norris Tammi, Maria L. Turner, Mark C. Udey, Martin A. Weinstock (ex officio) Exhibitors at the Annual Meeting Ad Hoc Reviewers American Skin Association, Inc., Blackwell Science, Inc., Candela Corpora- Elliot J. Androphy, Cheryl A. Armstrong, Angela M. Christiano, Ponciano tion, Dow Pharmaceutical Sciences, Ferndale Laboratories, Inc., Galderma D. Cruz, Jr., Vincent A. Deleo, Andrzej Dlugosz, Richard L. Eckert, James Laboratories, Inc., Spex Industries, Shandon Lipshaw, Coalition of Patient T. Elder, Craig A. Elmets, Kenneth R. Feingold, Richard L. Gallo, Barbara Advocates for Skin Disease Research, National Alopecia Areata Foundation, A. Gilchrest, Kathleen J. Green, Anne R. Haake, Russell P. Hall III, National Foundation for Ectodermal Dysplasias, PXE International, Inc., Robin Hornung, Pamela J. Jensen, Paul A. Khavari, Robert M. Lavker, Sturge-Weber Foundation Abstracts for the Annual Meeting of the International DermatoEpidemiology Association Sheraton Chicago Hotel, Chicago, Illinois May 6, 1999 Plenary and Concurrent Sessions Abstract Numbers Plenary and Concurrent Sessions Abstract Numbers Oral Session I01–I08 Poster Sessions (See SID Posters ‘‘Epidemiology/Health Services Inflammatory and Infectious Diseases I01–I02 Research’’ in this volume of the JID.) Skin Cancer/Melanoma I03–I06 Inflammatory and Infectious Diseases 824–832 Health Care Research I07–I08 Skin Cancer/Melanoma 833–835 Health Care Research 836–839 0022-202X/99/$10.50 · Copyright © 1999 by The Society for Investigative Dermatology, Inc. 522 VOL. 112, NO. 4 APRIL 1999 ABSTRACTS 523 001 002 Dendritic Cell Migration from Blood into Inflamed Skin Sites Prophylaxis and Therapy of Ongoing Immune Responses by IL-10-Treated Dendritic Cells In Vivo S. Grabbe,*† C. Robert,* R. C. Fuhlbrigge,* and T. S. Kupper* A. H. Enk, G. Mu¨ller, H. Jonuleit, K. Steinbrink, T. Tu¨ting, C. Szalma and J. Knop *Harvard Skin Disease Research Center, Harvard Medical School, Boston, Massachusetts; and Department of Dermatology, University of Mainz, Mainz, Germany †Department of Dermatology, University of Mu¨nster, Mu¨nster, Germany Treatment of immature dendritic cells (DC) with IL-10 is able to convert these antigen-presenting According to current paradigms, dendritic cells (DC) that reside in peripheral tissues internalize cells into tolerizing antigen-presenting cells in vitro. In order to assess whether IL-10-treated DC and present antigen both for priming of naı¨ve T cells as well as for elicitation of cell-mediated would also be able to induce tolerance in vivo we used a system of OVA-TCR-tg mice (DO11.10). immune responses. Since both mature DC and DC precursors are present in peripheral blood, we In these animals 40%–70% of all naı¨ve T cells express an ovalbumin-specific T cell receptor. To tested the hypothesis that circulating antigen-presenting cells may infiltrate inflamed skin and assess whether IL-10-treated DC would be able to prevent sensitization in these mice in vivo, thereby contribute to elicitation of antigen-specific cutaneous immune responses. For this purpose, murine bone-marrow derived DC were cultured fetal calf serum-free with GM-CSF/IL-4 and DC of various maturation stages were generated from murine bone marrow by culture in GM- treated with 30 ng rmIL-10 per ml starting at day 2 of culture. On day 5 cells were pulsed with CSF 6 IL–4 6 LPS and labeled with either a radioactive (51Cr) or a fluorescent (calcein) marker. 50 µg oxazolone (OVA) per ml. OVA-pulsed IL-10-DC and Ag-pulsed control DC, as well as Labeled DC were then injected i.v. into mice that were either sensitized and challenged with the unpulsed DC were injected into the tail vein of DO11.10 mice. Eight days later, mice were hapten oxazolone or challenged with the irritant phorbol ester PMA. Six hours later, ears and subcutaneously immunized with 30 µg OVA-peptide in IFA. Again 10 d later, total lymph node lymphatic organs were excised and analyzed for the presence of labeled DC. A small but significant cells (LNC) were harvested and restimulated with the OVA-peptide or a control peptide in vitro. immigration of circulating DC into inflamed skin was observed. No specific label was found in While good proliferative responses were observed in animals pretreated with Ag-pulsed DC or regional lymph nodes 6 h after injection, or in the skin after injection of nonviable DC or control unpulsed DC or even in controls that were only immunized subcutaneously, LNC from mice cells. DC extravasated into inflamed skin about five times more efficiently than into uninflamed that had received IL-10-treated Ag-pulsed DC showed only minimal response to peptide challenge. skin. Immature DC, generated by incubation in GM-CSF 1 IL-4 for 4 d, as well as the immature Thus pretreatment of OVA-tg mice with IL-10-DC prevents sensitization in vivo. To see, whether DC line XS52, homed most efficiently to sites of allergic contact dermatitis and less well to sites IL-10-DC can also downmodulate ongoing immune responses, DO11.10 mice were sensitized of irritant dermatitis. Preincubation of DC with TGFb1 further enhanced homing of immature by s.c. injection of OVA-peptide in IFA. Eight days later, T cells from sensitized tg-mice were DC to inflamed skin. Interestingly, mature DC lost their capacity to home to inflamed tissues. harvested and sorted for OVA-TCR T cells. Five 3106 of these T cells were injected i.v. into DC homing was observed as early as 2 h after oxazolone challenge and peaked at 6–8 h. normal BALB/C mice. Again 2 d later, these animals received either OVA-pulsed IL-10DC, Extravasation of DC into inflammatory skin sites was clearly detectable by confocal microscopy OVA-pulsed, or unpulsed control DC. Seven days later, total LNC from these animals were of anti-CD31-labeled cutaneous vessels and calcein-labeled DC. Thus, dendritic antigen-presenting harvested and restimulated with OVA peptide in vitro. LNC from animals from control mice cells extravasate from blood into inflamed skin and may thus play a role in elicitation or persistence showed a significant proliferation towards OVA peptide, while proliferation in T cells from mice of T cell-mediated skin disorders. pretreated with IL-10-DC was inhibited by 70%. These data indicate that IL-10-DC are able to downmodulate ongoing immune reactions in vivo. Further experiments are necessary to explain the mechanism of inhibition or tolerance in this system. 003 004 Anti-Tumor Immunity Induced by Immunization with RNA-Pulsed Epidermal Cells Dendritic Cells Function as Antigen-Presenting Cells in GM-CSF-Based Melanoma Vaccines R. D. Granstein and W. Ding A. Schneeberger, P. Lu¨hrs, R. Kutil, H. Schild,* P. Steinlein,† and G. Stingl Department of Dermatology, Weill Medical College of Cornell University, New York, New York DIAID, Department of Dermatology, University of Vienna Medical School, Vienna, Austria; RNA-pulsed dendritic cells can reportedly be used to immunize against antigens encoded for by †Research Institute of Molecular Pathology, Vienna, Austria; *Department of Immunology, the RNA utilized. As the epidermis contains dendritic antigen-presenting cells (Langerhans cells) Laboratory of Cell Biology, University of Tu¨bingen, Germany and is a convenient site for immunization strategies, we asked if epidermal cells (EC) enriched for We and others could recently demonstrate that the injection of GM-CSF-expressing cancer cells Langerhans cell content could be used to immunize mice against the S1509a spindle cell tumor into experimental animals leads to a protective, T cell-mediated antitumor immune response.